Introduction of Rotavirus:
Rotaviruses are responsible for significant gastrointestinal disease, primarily in children 5 years of age and the young of other mammalian species. By the age of five, almost all children worldwide suffer from rotavirus gastroenteritis; 1 in 5 visit a clinic, 1 in 65 are admitted to the hospital, and 1 in 293 may away.
Morphology of Rotavirus:
The virus has a three-layer, icosahedral capsid without an envelope, and its diameter is 70 nm. The outer capsid’s well-defined circular form resembles the rim of a wheel set on short projections that extend from a broad arm. The virus is called “rota” (a Latin word meaning wheel) because of this appearance.
The genome is made up of eleven double-stranded RNA segments. The virus’s eleven double-stranded RNA segments are encased in three protein shells: an internal core, an outer capsid, and an inner capsid.
The P and G serotypes are defined by the outer capsid proteins VP4 and VP7, which are neutralization antigens. The subgroup antigen is the inner capsid structural protein, or VP6. Viral protein (VP7), a large glycoprotein with a molecular weight of 34,000 Da, makes up the outer shell. Additionally, it contains a small trypsin-sensitive protein known as VP4, which has a molecular weight of 84,000 Da. VP1, VP2, VP3, and VP6 are the four proteins that make up the minor shell or core protein of the virus core. Six nonstructural proteins are also present in the virus.
Rotavirus Subgroups, Groups, and Serotypes:
- Although 11 G serotypes of HRVs have been found, the great majority have been classified as G1, G2, G3, or G4, and strains from these G types are typically referred to as serotypes 1, 2, 3, or 4, correspondingly.
- There is little to no variation in the degree of sickness induced by viruses belonging to these four serotypes. There are at least six distinct HRV P types known. The most prevalent P type 1a is typically linked to G types 1, 3, or 4, while P type 1b is typically linked to G type 2.
- Based on the electrophoretic mobility of the genomic segments and antigenicity of VP6, rotaviruses are divided into seven groups (A through G). Group A rotaviruses are primarily responsible for human disease, with group B and C rotaviruses sometimes occasionally causing illness.
Replication cycle of Rotavirus:
The entire process of replication is cytoplasmic. Because cells lack the enzymes needed to generate dsRNA, the virus must give them. Transcripts serve as a template for the synthesis of negative-strand RNA in addition to producing proteins. The complementary negative strand stays connected to the positive strand once it is created. Free dsRNA or free negative stranded ssRNA is typically absent from infected cells, and the dsRNA segments are created within developing subviral particles. Cytoplasmic viroplasms are the site of RNA replication. Subviral particles develop alongside viroplasms and mature by budding through the ER membrane. Particles pick up their outer capsid proteins during this step. The regulation of viral assembly and particle integrity depends on intracellular calcium levels. Infected cells cultivated on monolayers release particles through cell lysis.
Pathophysiology of Rotavirus Infection:
- Feco-oral transmission is route of rotavirus spread. Rotavirus begins to infect the mucosal cells of the small intestine after surviving in the stomach’s acidic environment. Following absorption, the viruses disrupt the enterocytes’ transport system by replicating in their cytoplasm.
The rotavirus’s non-structural protein 4 (NSP4) may function as a viral enterotoxin that induces fluid secretion by activating a signal transduction pathway. The toxin causes enterocytes to absorb calcium ions, releases neural activators, and modifies the absorption of glucose and sodium. - Because injured cells on the villi are replaced by non-absorbing immature crypt cells, the resultant diarrhea is caused by reduced absorption of glucose and salt. After multiplying within the cell, the rotavirus damages the cell. Large amounts of viruses are produced in the diarrheal stool as a result of the injured cells being discharged into the intestinal lumen. Restoring the cell’s normal function takes between three to eight weeks. As a result, the rotavirus causes watery diarrhea that resembles cholera.
Clinical Manifestations:
One of the main causes of diarrhea in newborns and young children is rotavirus.
The incubation time is brief—less than 48 hours.
Frequent symptoms of the illness include fever, vomiting, diarrhea, and occasionally dehydration.
Vomiting can happen either before or after the onset of diarrhea and is often brief.
There is no mucus in the diarrheal stool, which might be watery, green, or yellow.
Patients with rotavirus diarrhea fully recover in 5–10 days without experiencing any problems or after-effects since the illness is self-limiting. Additionally, rotavirus has been identified as a cause of adult traveler’s diarrhea. Adult cases of gastroenteritis have also been linked to the virus.
Treatment and Management:
There is no particular antiviral treatment for rotavirus infections. The majority of the condition’s treatment is supportive. It entails replenishing the lost fluid in patients who are dehydrated.
In order to restore hydration, oral rehydration fluid with glucose and electrolyte solution is currently preferred over intravenous fluids. Only children who are extremely dehydrated should receive intravenous fluids.